Diabetes Flashcards
What are two physiological causes of diabetes
- Decreased insulin secretion/insulin deficiency
- decreased insulin sensitivity/insulin resistance
Could be caused by either or both.
Chronic hyperglycemia leads to
Organ and nerve damage throughout the body
Insulin is
a hormone produced by beta islet cells in the pancreas, which helps bring glucose from blood to muscle, and excess is stored in the liver (glycogen) and fat cells (FFA) for energy reserve
What is glycogen
Produced in the muscle and liver through glycogenesis to help store glucose (signaled by insulin)
What is glucagon, how does it work
A hormone that works the opposite way as insulin and is produced by alpha cells in the pancreas. Released when BG is low, it helps the liver to start glycogenolysis and release glucose into the blood stream. In fat tissue it signals FFA’s to make ketones
What happens when glycogen is depleted
Glucagon is released and acts on fat tissue to cause FFA’s to make ketones, and ketones are used as energy
What is type 1 diabetes
~5% of cases- mostly dx in children
- autoimmune destruction of beta islet cells and insulin can’t be produced
- Family history is the largest risk factor
- must tx with insulin
-screen for other autoimmune disorders like celiac and thyroid issues
Patients commonly present with DKA and then are diagnosed
What is diabetic ketoacidosis (DKA)
When the body is not storing glucose from the blood into cells, so the BG is so high, and the cells are so hungry, that the glucagon is released to fat tissue to metabolize FFA into ketones at high amounts.
This is often the initial presentation for T1DM
How do we test and see if a person has T1DM
C- peptide test
- it is released by the pancreas only when the pancreas actually releases insulin
- if very low levels, we dx T1DM
What is T2DM
- Caused by both insulin resistance and insulin deficiency
- Beta islet cells become damaged over time and make less insulin
- onset of disease often unnoticed because hyperglycemia develops gradually; older patients are dx
- assoc. with obesity, FH, physical inactivity, and other comorbidities
- tx with lifestyle modifications in few, most +/- medications
What is prediabetes and how do we treat?
A1c% = 5.7-6.4
FBG = 100-125
2hrPP = 140-199
Prevention of progression: diet and exercise, monitor DM progression annually and treat CVD risk factors
Could treat with metformin to improve BG levels esp. if they have these risk factors: BMI is > 35 , they are < 60 yrs, or they had a hx of gestational DM
What happens to mothers and babies
when gestational diabetes occurs
- Mother is tested between 24-28 weeks using OGTT, hyperglycemia should be treated with lifestyle modifications and medication if needed ( insulin preferred then metformin or glyburide)
-babies are larger than normal (macrosomia) and at higher risk for obesity and diabetes later - the mother is more likely to develop T2DM later and the babies BG is likely to go too low right after birth bc no longer depending on mothers BG
- Mother’s BG goals are very strict (no A1c goal, but fasting </= 95, 1hr PPG </=140, 2hrPPG </=120)
What are patient criteria where we could start metformin
- prediabetes (A1c% 5.7-6.4 or FBG: 100-125, or 2HRPP: 120-189
-BMI >/= 35 kg/m^2 - younger than 60
- history of gestational DM (GDM)
we should monitor annually for the development of diabetes and treat modifiable risk factors
Risk factors for prediabetes and T2DM diabetes
- lack of physical activity*
- overweight (BMI > 25 kg/m2 or 23 in Asian Americans)*
- central obesity (fat in tummy)
- high risk race or ethnicity: anyone who’s not white*
- history of gestational diabetes*
- A1C > 5.7%*
- first degree relative with diabetes*
- HDL < 35 mg/dL or TG > 250 mg/dL
- HTN (>/=140/90 mmHg) or taking BP meds
- CVD history
- Smoking history
- Condition that causes insulin resistance (acanthosis nigricans, PCOS)
Symptoms of hyperglycemia
- the P’s: excessive urination (polyuria), thirst (polydipisia), and hunger (polyphagia)
- fatigue
- blurry vision
- erectile dysfunction (due to vessel destruction) (note: when someone has ED we may check if they also have DM or Cardiovascular issues)
- vaginal fungal infections
Screening for diabetes
- risk for T2DM increases with age, so test everyone starting at age 35
- test all asymptomatic children, adolescents, and adults who are overweight > 25 BMI or 23 in asian Americans and have at least one other risk factor for diabetes; if normal retest q3yrs
How is T2DM diagnosed
- Lab sent Hemoglobin A1c test (>6.5%) tells the average BG in past 3 months or
- Fasting plasma glucose (FPG) (>/= 126 mg/dL) at least 8 hrs post meal or
- OGTT (>/= 200 mg/dL) 2 hrs after drinking glucose liquid
None are preferred more than another, but for FPG and A1C we must get two abnormal results from the same or different tests to confirm diagnosis UNLESS we also have a clear clinical dx. (e.g. classic symptoms of hyperglycemia + BG >/= 200)
Point of care A1c tests are NOT recommended for diagnosing.
Treatment goals for DM (non pregnant)
Non pregnant:
A1c : < 7 or 6.5 if possible without significant hypoglycemia or <8 if the person has low life expectancy or gets severe hypoglycemia; test q3months if not at goal and q6 months if at goal
Preprandial BG: 80 - 130 mg/dL
2 hr PPG: < 180 mg/dL
Treatment goals for Gestational DM
- Mother’s BG goals are very strict (no A1c goal, but fasting </= 95, 1hr PPG </=140, 2hrPPG </=120)
What is the relationship between A1c and eAg
A1c of 6% = eAg of 126 mg/dL, for every increase in A1c by 1%, there is a 28 mg/dL increase in estimated average glucose
ex: A1c of 7% means the eAg is 126 + 28 = 154 mg/dL
What lifestyle modifications can we education patients on to lower BG, improve cholesterol, and BP?
- Goal waist circumference of <35 inches in females, <40 inches in males
- Overweight or obese pts should lose > 5% of their body weight and medications or surgery can help
- Consume natural carbs, avoid or limit alcohol (can hinder insulins act and lead to DKA)
- T1DM patients should use carbohydrate counting with mealtime (prandial) doses (15 g carbs = 1 slice of bread, 1/3 cup of rice/pasta, or 1 piece of fruit)
- at least 150 minutes of moderate exercise/week and reduce sedentary lifestyle by standing every 30 min at least.
- quit smoking
What long term complications can we prevent with glycemic control?
Macrovascular diseases (same as atherosclerotic cardiovascular disease - ASCVD) : large vessels
- CAD (ex: MI, atherosclerosis, different heart diseases)
- Cerebrovascular disease (ex: stroke)
- Peripheral artery disease (PAD) - like atherosclerosis in vessels of leg
Microvascular diseases: small vessels
- retinopathy
- diabetic kidney disease (nephropathy)
- peripheral neuropathy (loss of sensation/tingling) & increased risk of foot infections and amputations
- autonomic neuropathy (gastroparesis, loss of bladder control, erectile dysfunction)
Diabetes is the top cause of what three complications? and what is the primary cause of death of DM patients?
- lower extremity amputations
- kidney failure
- blindness
- primary cause of death is CVD - occurs at 2-4 times more than regular ppl’s cause of death
ASCVD prevention for DM patient
Can give ASA 75-162 mg/day - typically just 81 mg/day for secondary prevention only (ex: after MI)
Can give clopidogrel 75 mg daily if they have an allergy to ASA
DM patient with CAD or PAD can be given what to prevent complications
ASA 81 mg/day PLUS xarelto
How can we reduce risk of secondary pre-eclampsia in pregnancy
- Give ASA 81 mg daily starting after 12 weeks in women at risk for preeclampsia
How can we monitor for diabetic retinopathy
Patients should get an eye exam using dilation at the time of DM diagnosis
- If they have retinopathy; repeat eye exams every year
- If they don’t; repeat eye exams every 1-2 years